Rational treatment of corneal wounds and recurrent corneal erosions requires an understanding of the repair processes of the cornea. During corneal wound healing epithelial cells move to cover the defect. After the wound is covered the cells develop specialized adhesion organelles (hemidesmosomes) with the basement membrane. Recent advances in cell biology demonstrate the presence of the proteins actin and myosin in non-muscle cells, and evidence is accumulating that these proteins are involved in non-muscle cell motility. We have recently demonstrated that of 7-12% of total protein in both normal corneal epithelial cells and in cells migrating to cover corneal abrasions is actin. There is, however, a striking change in the distribution of actin filaments between the two cell states. These studies also demonstrated that the distribution of two other cytoskeletal filaments in corneal epithelium, tonofilaments and microtubules, changes dramatically in the transition from normal to migrating. We propose to do a correlated biochemical and histochemial study on the role and interaction of tonofilamets, microtubules, and actin filaments in corneal epithelial wound healing. We will employ techniques of electrophoresis and immunofluorescence microscopy for the in vitro study of rat epithelial cell migration. In addition we will begin to probe the characteristics of basement membranes that facilitate or inhibit migration and hemidesmosome formation by blocking specific sugar sites on the basement membrane with lectins. We will look at the effects of motility inhibitors (local anesthetics) and stimulators (epidermal growth factors and ions) on the cytoskeletal and contractile filaments and upon hemidesmosome formation. These studies will ultimately be related to the development of better treatments for corneal wounds and to the elucidation of the etiology of recurrent corneal erosions.